Chromium chloride

Cat. No.: HY-B1608 Purity: 99.9%: Data Sheet
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Chromium chloride is a trivalent chromium compound and an essential trace mineral. Chromium chloride enhances insulin-stimulated GLUT4 translocation and glucose uptake in skeletal muscle. Chromium chloride regulates glucose and lipid metabolism, inhibits TNF-α secretion and oxidative stress in monocytes treated with high glucose or H₂O₂, and reverses hydrogen peroxide-induced cell growth inhibition. Chromium chloride reduces coronary and aortic lipid deposition and serum cholesterol levels in hypercholesterolemic rabbits. Chromium chloride can be used in research related to diabetes and cardiac atherosclerosis.

For research use only. We do not sell to patients.

Chromium chloride Chemical Structure

CAS No. : 10025-73-7

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Biological Activity
Purity & Documentation
References
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Description

In Vitro

Chromium chloride (1-1000 μM; 24 h) concentration-dependently inhibits elevated TNF-α secretion in high glucose-treated, PMA/lipopolysaccharide-activated U937 cells, with significant inhibitory effects observed across the concentration range after 24 h^[2].
Chromium chloride (1-1000 μM; 24 h) inhibits elevated TNF-α secretion in H₂O₂-treated, PMA/lipopolysaccharide-activated U937 cells, with significant inhibitory effects observed across the concentration range after 24 h^[2].
Chromium chloride (10-1000 μM; 24 h) prevents H₂O₂-induced growth inhibition in U937 cells, with significant protective effects observed across the concentration range after 24 h^[2].
Chromium chloride (100 μM; 24 h) inhibits elevated lipid peroxidation levels in both high glucose-treated and H₂O₂-treated U937 cells after 24 h^[2].
Chromium chloride (100 μM; 24 h) inhibits elevated protein oxidation levels in both high glucose-treated and H₂O₂-treated U937 cells after 24 h^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ELISA Assay^[2]

Cell Line:	human promonocytic U937 cells (PMA/lipopolysaccharide-activated, high glucose-treated)
Concentration:	1, 10, 100, 1000 μM
Incubation Time:	24 h
Result:	Inhibited elevated TNF-α secretion in a concentration-dependent manner, with statistically significant reductions (P < 0.02) observed at all tested concentrations compared to the high glucose-only control.

ELISA Assay^[2]

Cell Line:	human promonocytic U937 cells (PMA/lipopolysaccharide-activated, hydrogen peroxide-treated)
Concentration:	1, 10, 100, 1000 μM
Incubation Time:	24 h
Result:	Inhibited elevated TNF-α secretion at all tested concentrations, with statistically significant reductions (P < 0.02) observed compared to the H2O2-only control.

Cell Proliferation Assay^[2]

Cell Line:	human promonocytic U937 cells (hydrogen peroxide-treated)
Concentration:	10, 100, 1000 μM
Incubation Time:	24 h
Result:	Prevented H2O2-induced growth inhibition at concentrations of 10, 100, and 1000 μM, with statistically significant differences (P < 0.01) observed compared to the H2O2-only control.

In Vivo

Chromium chloride (1 mg (0.33 mg chromium/kg body weight); i.m.; 6 days per week; 6 weeks) significantly reduces coronary and ascending aortic lipid deposits, as well as serum cholesterol, in hypercholesterolemic New Zealand white rabbits, while causing reversible liver function test abnormalities without significant histopathological liver or kidney damage^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	New Zealand white rabbits (male adult, aged 15 weeks, initial weight 2683.6 g; hypercholesterolemic induced by 2% cholesterol diet for 30 days)^[3]
Dosage:	1 mg chromium chloride (0.33 mg chromium/kg body weight)
Administration:	i.m.; 6 days per week; 6 weeks
Result:	Reduced mean log₁₀(ORO+1) value (coronary lipid deposit area) to 1.5253, which was significantly lower than untreated hypercholesterolemic rabbits. Reduced mean area of ascending aortic lipid deposits to 255.552, which was significantly lower than untreated hypercholesterolemic rabbits. Reduced terminal mean serum cholesterol concentration to 175.180 mg/dL, which was significantly lower than untreated hypercholesterolemic rabbits. Increased terminal mean serum chromium concentration to 3746.4 μg/L, compared to 4.3 μg/L in untreated rabbits. Reduced serum albumin level to mean 48.63 g/L, alkaline phosphatase to mean 35.50 U/L, triglyceride to mean 1.07 mmol/L, and HDL-C to mean 0.66 mmol/L relative to untreated hypercholesterolemic rabbits. Showed no significant histopathological differences in liver or kidney between chromium chloride-treated and untreated hypercholesterolemic rabbits.

Clinical Trial

Molecular Weight

158.36

Formula

CrCl₃

CAS No.

10025-73-7

Appearance

Solid

Color

Pale purple to purple

SMILES

Cl[Cr](Cl)Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

Purity & Documentation

Purity: 99.9%

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Data Sheet (281 KB) SDS (759 KB)

COA (254 KB)

Handling Instructions (2659 KB)

References

[1]. Doerner PG 3rd, et al. Chromium chloride increases insulin-stimulated glucose uptake in the perfused rat hindlimb. Acta Physiol (Oxf). 2014;212(3):205-213.

[2]. Jain SK, et al. Chromium chloride inhibits oxidative stress and TNF-alpha secretion caused by exposure to high glucose in cultured U937 monocytes. Biochem Biophys Res Commun. 2001;289(3):687-691.

[3]. Price Evans DA, et al. Chromium chloride administration causes a substantial reduction of coronary lipid deposits, aortic lipid deposits, and serum cholesterol concentration in rabbits. Biol Trace Elem Res. 2009;130(3):262-272.